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Emancipation from transcriptional latency: unphosphorylated STAT5 as guardian of hematopoietic differentiation
Author(s) -
Decker Thomas
Publication year - 2016
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201693974
Subject(s) - stat5 , biology , phosphorylation , transcription factor , tyrosine phosphorylation , stat , janus kinase , microbiology and biotechnology , stat3 , genetics , gene
The canonical paradigm of Jak‐STAT signaling is that members of the signal transducers and activators of transcription ( STAT s) family of transcription factors are activated by Janus kinase (Jak)‐mediated tyrosine phosphorylation. While the relationship between activation and tyrosine phosphorylation still appears axiomatic, several lines of evidence suggest that unactivated, unphosphorylated isoforms, uSTAT s, are nonetheless also engaged in transcriptional regulation. In this issue of The EMBO Journal , Park et al (2015) make a convincing case that nuclear uSTAT 5 controls hematopoietic differentiation.